Synovial PMN show a coordinated up-regulation of CD66 molecules

Abstract

Changes in the expression of various activation-dependent surface markers have been reported for polymorphonuclear neutrophils (PMN) isolated from synovial fluid of patients with inflammatory joint diseases. We extend these findings to the expression of CD66 molecules and several other surface markers. Three members of the CD66 family, namely CD66a, CD66b, and CD66c, showed an up to fourfold up-regulation on synovial fluid PMN compared with peripheral blood PMN (PBG) of the same patients; CD59 was increased twofold, the expression of CD16 did not change, whereas CD62L was reduced by more than 50% on synovial fluid PMN. It is interesting that CD66a, CD66b, and CD66c showed a coordinated expression on PBG of patients and controls and a coordinated up-regulation on synovial neutrophils. In contrast, after in vitro stimulation of peripheral blood PMN with phorbol myristate acetate, CD66c was much less up-regulated compared with CD66a and CD66b. All samples of synovial fluid PMN exhibited an additional increase in the expression of CD66a, CD66b, and CD66c when stimulated with phorbol myristate acetate in vitro. Prostaglandins are known to inhibit various responses of neutrophils to inflammatory stimuli. We could show that prostaglandins inhibit N-formyl-methionylleucyl-phenylalanine-induced up-regulation of CD66 on peripheral blood PMN in a concentrationdependent manner. J. Leukoc. Biol. 66: 429-436; 1999.

Regulation of leukocyte adhesion molecules by leukocyte/biomaterial‐conditioned media: A study with calcium‐phosphate‐coated and non‐coated NiTi‐shape memory alloys

“…The pattern in the regulation of the analyzed adhesion molecules observed in the present study clearly fits into results on regulation of adhesion molecules after leukocyte activation induced by cytokines [8,13,14].…”

“…As previously reported we also detected high levels of cytokines (IL-6, IL-8, GM-CSF) within conditioned media obtained by the interaction of leukocytes with CaP-coated samples in contrast to respective conditioned media where noncoated samples were used [6]. Furthermore, the upregulation of CD66b on PMN within inflamed synovial fluid has been shown [14] indicating the regulation of adhesion molecules by soluble mediators in vivo.…”

“…CD66b carcinoembryonic antigen-related cell adhesion molecule obviously plays a role in the interaction between granulocytes or between granulocytes and epithelial cells [14].…”

Release of the Soluble Urokinase-Type Plasminogen Activator Receptor (suPAR) by Activated Neutrophils in Rheumatoid Arthritis

“…To confirm the activated state of SF neutrophils in our preparations, we analyzed the surface expression of three membrane markers of inflammatory activation, L-selectin (CD62L), CD66b and CD11b, on freshly isolated PB and SF neutrophils (Table 1). Neutrophil extravasation and migration into the inflamed tissue leads to L-selectin shedding and concomitant translocation of CD66b and CD11b from intracellular mobilizable compartments onto the plasma membrane [29][30][31]. As expected, L-selectin surface expression was significantly diminished on SF neutrophils (Table 1) consistent with L-selectin shedding upon granulocytes transmigration into the inflamed areas [29].…”

Transdifferentiation of polymorphonuclear neutrophils to dendritic-like cells at the site of inflammation in rheumatoid arthritis: evidence for activation by T cells

“…6 7 Furthermore, in numerous studies evidence for activation of PMN in synovial fluid (SF) has been reported, particularly the modulation of activation associated surface receptors, including for example, CD66a-c, CD35, CD46, or CD11a/b. [8][9][10] Because PMN have a reservoir of receptors and cytokines, and a propensity to generate and release cytotoxic and proteolytic entities, they may contribute to cartilage destruction. Numerous reports on the role of PMN in the development of tissue damage have been published, including, for example, lesions occurring in ischaemia reperfusion and lung injury, 11 12 in the development of chronic wounds, 13 or in chronic inflammatory diseases, including RA.…”